Skip to main content
eScholarship
Open Access Publications from the University of California

Hipk2 cooperates with p53 to suppress γ-ray radiation-induced mouse thymic lymphoma

  • Author(s): Mao, JH
  • Wu, D
  • Kim, IJ
  • Kang, HC
  • Wei, G
  • Climent, J
  • Kumar, A
  • Pelorosso, FG
  • Delrosario, R
  • Huang, EJ
  • Balmain, A
  • et al.
Abstract

A genome-wide screen for genetic alterations in radiation-induced thymic lymphomas generated from p53 +-and p53-/-mice showed frequent loss of heterozygosity (LOH) on chromosome 6. Fine mapping of these LOH regions revealed three non-overlapping regions, one of which was refined to a 0.2 Mb interval that contained only the gene encoding homeobox-interacting protein kinase 2 (Hipk2). More than 30% of radiation-induced tumors from both p53 +-and p53-/-mice showed heterozygous loss of one Hipk2 allele. Mice carrying a single inactive allele of Hipk2 in the germline were susceptible to induction of tumors by γ-radiation, but most tumors retained and expressed the wild-type allele, suggesting that Hipk2 is a haploinsufficient tumor suppressor gene for mouse lymphoma development. Heterozygous loss of both Hipk2 and p53 confers strong sensitization to radiation-induced lymphoma. We conclude that Hipk2 is a haploinsufficient lymphoma suppressor gene. © 2012 Macmillan Publishers Limited All rights reserved.

Many UC-authored scholarly publications are freely available on this site because of the UC Academic Senate's Open Access Policy. Let us know how this access is important for you.

Main Content
Current View